.png){kind=icon}
.png){kind=icon}
Return
The PCK2-Traf6-Tollip Axis Restricts PEDV Replication by Orchestrating Selective Autophagic Degradation of the Viral Nucleocapsid Protein
.png){kind=icon}
OA
AI
A
X
W
D
Y
H
Z
童
S
N
L
DOI：10.1155/tbed/8776901.png)
.png){kind=icon}
.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
Porcine epidemic diarrhea virus (PEDV) is a devastating enteric pathogen in neonatal piglets, causing outbreaks with high mortality. The lack of effective vaccines or treatments makes elucidating host-pathogen interactions essential for developing control strategies. In this study, we identify phosphoenolpyruvate carboxykinase 2 (PCK2) as a host restriction factor that targets the viral nucleocapsid (N) protein for degradation, thereby suppressing PEDV replication. This PCK2-mediated antiviral effect was reversed by autophagy inhibitors, indicating the involvement of a selective autophagic. Mechanistically, we found that PCK2, the N protein, the E3 ubiquitin ligase Traf6, and the cargo receptor Tollip form a functional complex. Depletion of either Traf6 or Tollip disrupted the autophagy pathway, restored N protein stability, and consequently rescued viral replication from PCK2 inhibition. This study unveils a novel antiviral mechanism in which PCK2 orchestrates the selective autophagic degradation of the PEDV N protein, highlighting the PCK2-Traf6-Tollip axis as a promising therapeutic direction.
Keywords:
autophagy pathway
degradation
PCK2
PEDV N
AI Summary
Key information extracted from the uploaded paper, including a brief overview, abstract, background, key highlights, visual analysis, and future outlook.
Journal
IF:
3
Papers:
3.8K
Citations:
9.5K
Organization
Cited Papers